The phenomenon of human platelet injury by plasma-treated Histoplasma capsulatum will be analyzed in terms of plasma factor requirement, determining whether or not the alternate complement pathway is involved by heating plasma at 50 degrees C, and using MgEGTA in the plasma treatment phase. The requirement for fibrinogen will be investigated by determining the effectiveness of various components of the fibrinogen molecule in supporting this type of platelet injury. Aggregation of isolated platelets in buffer by plasma-treated H. capsulatum will be studied to determine the configuration of the aggregation trace, and the role of platelet ADP. B. dermatitides, C. neoformans, and C. albicans yeasts will be studied in the same system. The ability of supernates from cultures of lymphocytes from histoplasmin-sensitive individuals and H. capsulatum will be assayed for the property of producing aggregation and release of serotonin from plasma-free platelet in buffer.